Oxidative stress and fibrosis-related pathways

Oxidative stress and fibrosis-related pathways represent a complex network of biological processes where an imbalance between reactive oxygen species (ROS) and antioxidant defenses leads to cellular damage and the pathological accumulation of extracellular matrix [PMID: 22503688]. These pathways are central to the pathogenesis of various chronic diseases, including idiopathic pulmonary fibrosis, chronic kidney disease, and liver cirrhosis [PMID: 30213014]. Key molecular players often include the transforming growth factor-beta (TGF-beta) signaling cascade, NADPH oxidases (NOX), and the Nrf2-Keap1 antioxidant response system [PMID: 24561458]. Therapeutic strategies targeting these pathways aim to reduce oxidative damage and inhibit the activation of myofibroblasts, thereby slowing or reversing tissue scarring [PMID: 26338313]. However, because these pathways are integral to normal wound healing and cellular signaling, achieving specificity without disrupting homeostatic functions remains a significant challenge in drug development [PMID: 28855243].

Other names

Redox-fibrosis axisOxidative stress-mediated fibrogenesisFibrogenic oxidative signalingROS-TGF-beta signaling axis

Modulation of reactive oxygen species (ROS) levels and inhibition of pro-fibrotic signaling cascades such as the TGF-beta/Smad pathway.